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SRNAPharmacology II > Comprehensive Review > Flashcards

Comprehensive Review Flashcards

1
Q

What adverse effects are associated with the use of aminoglycosides?

A

a. Nephrotoxicity-
b. Ototoxicity
c. Neurotoxicity-

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2
Q

With Nephrotoxicity with aminoglycosides there is

A

decreased creatinine clearance, casts in urine (chunks of glomerulus), decreased specific gravity, oliguria, proteinuria

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3
Q

With ototoxicity with aminoglycosides there is

A

directly r/t duration > 10 days & concurrent administration of ototoxic drugs

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4
Q

With neurotoxicity with aminoglycosides there is

A

skeletal muscle weakness, inhibits pre-junctional release of Ach & decreased postsynaptic sensitivity to Ach- potentiates NMB. *Caution with Parkinson & Myasthenia
Gravis, IV Ca+ can counteract

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5
Q

Examples of Aminoglycosides are

A

Amikacin, Gentamicin, Neomycin Streptomycin, &

Tobramycin

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6
Q

What is common adverse reaction associated with the use of Tetracyclines? (Doxycycline, Minocycline, Demeclomycin)

A

a. Photosensitivity
b. Vestibular symptoms with MINOCYCLINE
c. Deposition in teeth in pediatrics (stains teeth permanently)

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7
Q

Vestibular symptoms associated with

A

minocycline

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8
Q

What is the recommended time of administration of cefazolin (1st Gen) for prevention of post-op
infections?

A

a. Give pre-op in OR before induction, no sooner than 1 hour prior to procedure
b. Infuse over 3-5 min
c. <120 kg = 2 g IV, >120 kg = 3 g IV

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9
Q

What is the percentage of cross reactivity between penicillins and cephalosporins?

A

a. Approximately 5%

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10
Q

What may result if vancomycin is infused too fast?

A

a. Red Neck or Redman Syndrome

b. Clinical signs/symptoms- Histamine release (Non-Immune mediated *Barash) & hypotension

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11
Q

What can prevent red neck redman syndrome with vanco

A

*Give over 60 minutes to reduce this phenomenon

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12
Q

What NMB can Vancomycin potentiate?

A

a. Succinylcholine

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13
Q

Adverse reactions of Vancomycin?

A

a. Nephrotoxicity
b. Ototoxicity (would be at a disadvantage if we added this with an aminoglycoside)
c. Allergic Reactions

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14
Q

What antibiotics are classified as beta-lactams?

A

PCN, Cephalosporins, Imipenem/ Cilastin, Meropenem, Aztreonam is a monobactam, Carbapenems

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15
Q

Which antibiotics are associated with prolongation of neuromuscular blockade?

A

Aminoglycosides, Polymyxin B

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16
Q

What antibiotics are associated with prolongation of the QTc interval?

A

Macrolides (Erythromycin, Clarithromycin, Azithromycin), Vorconazole (antifungal)

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17
Q
  1. What antibiotic can be used if patient has an allergy to penicillin and cephalosporin?
A

a. Aztreonam (only gram -)

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18
Q

What are some adverse reactions of Cephalosporins?

BPHRH

A

a. Bleeding (prolonged PT)
b. Hypersensitivity
c. Pseudomembranous colitis
d. Renal Impairment
e. Hepatic Impairment with Cefoperazone

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19
Q

What is an adverse reaction of Chloramphenicol?

A

a. Aplastic Anemia

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20
Q

Use of Chloremphenical is

A

Use is limited to Typhoid Fever & Salmonellosis (if alternatives are less effective)

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21
Q

Define zero order kinetics.

A

A fixed/constant amount of drug is eliminated/unit of time

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22
Q

Define Hoffman degradation.

A

Spontaneous degradation via temperature & pH (Acidosis & Cold prolongs)

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23
Q
  1. What drugs undergo zero order kinetics?
A

a. ETOH, ASA, phenytoin, heparin, warfarin, acetaminophen

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24
Q

Define first order kinetics?

A

a. A percentage (%) or fraction of drug is eliminated/unit of time

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25
Q

Define half-life.

A

a. Time it takes for plasma concentration to fall by half

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26
Q

How are clearance, VD and half-life related?

A

Half-life is directly related to Vd and inversely related to clearance

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27
Q

Large volume of distribution =

A

long half-life

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28
Q

Increase in clearance =

A

Decrease in half-life

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29
Q

What opioids are most effective for the treatment of post-op shivering?

A

a. Meperidine (via Kappa), butorphanol (Stadol),

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30
Q

Clonidine as far as shivering

A

effective than meperidine

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31
Q

Which narcotic agonist have the shortest effect site equilibration time?

A

a. Alfentanil (1.4 min), Remifentanil (1.1)

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32
Q

What are common adverse effects associated with the use of narcotics?

A

Respiratory depression, N/V, urinary retention, pruritus

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33
Q

Can exacerbate CO2 narcosis

A

Opiods

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34
Q

Which opioid agent can blunt the adrenal response to stress?

A

Fentanyl

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35
Q
  1. How are opioid receptors classified?
    a. Mu1 (supraspinal & spinal)-
    c. Delta (supraspinal & spinal)- antidepressant effects, physical dependence, vent depression,
    constipation (minimal), urinary retention, modulates Mu receptor activity. Agonist- enkephalins,
    no delta selective agents. Antagonists- naloxone.
    d. Kappa (supraspinal & spinal)- analgesia, sedation, dysphoria, low abuse potential, miosis,
    diuresis.
A

produces analgesia, euphoria, decreased abuse potential, miosis, urinary retention, hypothermia. Agonists- endorphins, morphine, synthetic opioids. Antagonistnaloxone

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36
Q

Mu2 (spinal only)-

A

analgesia, hypoventilation, physical dependence physical dependence. Agonists- endorphins, morphine, synthetic opioids.

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37
Q

Constipation (marked),

A

Mu 2

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38
Q

Dysphoria and Diuresis with

A

Kappa

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39
Q

Mu 2 agonists

A

Endorphins, morphine, synthetic opioids.

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40
Q

OPIOID AGONIST-ANTAGONISTS principally work here. A

A

Kappa

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41
Q

Agonists-

A

Dynorphins (inhibit NT release via type N Ca++ channel causing analgesia, decreased resp. depression, may cause diuresis & dysphoria, increased intensity antagonist- naloxone.

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42
Q

Painful simulation may be resistant to analgesic effects of

A

kappa receptors,

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43
Q

Low abuse potential which receptors

A

Kappa

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44
Q

Constipation (minimal)

A

Delta

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45
Q

Antidepressant effects,

A

Delta (supraspinal & spinal)-

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46
Q

Physical dependence

A

Mu2

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47
Q

Which induction agent is associated with increases in ICP?

A

Ketamine

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48
Q

Which induction agent can blunt the adrenal response to stress?

A

Etomidate

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49
Q

Caution in adrenal insufficiency patient’s

A

Etomidate

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50
Q

Which induction agents possess analgesic properties?

A

Ketamine

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51
Q
  1. What is the mechanisms of action of:
    Etomidate-
    e.
A

binds GABA, enhances affinity of GABA receptor

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52
Q

What is the mechanisms of action of Propofol?-

A

activates GABA, increases Cl ions- hyperpolarizes cell, functional inhibition, decreases rate of GABA dissociation

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53
Q

What is the mechanisms of action of Dexmedetomidine-

A

Central alpha-2 agonist (Can cause bradycardia and hypotension)

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54
Q

What is the mechanisms of action of Ketamine

A

Non-competitive NMDA antagonist, weak GABA actions?, interacts with mu, delta, kappa receptors, muscarinic antagonist, K and Ca channels

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55
Q

What is the mechanisms of action of benzo

A

Benzodiazepines- different from barbs- enhance affinity of GABA receptor for GABA, by binding/

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56
Q

The benzos increase the

A

frequency of GABA-mediated ion channel opening and increase Cl permeability and thus cause cellular hyperpolarization and inhibition of neuronal firing

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57
Q

Barbiturates-

A

Binds to GABA-A receptor at barb binding site and increases GABA mediated Cl influx- hyperpolarizes
cell membrane

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58
Q

Decreases dissociation of GABA, increases duration of GABA activation,

A

Barbiturates

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59
Q

Depresses RAS, depresses SNS transmission, decreases sensitivity of Ach receptors.

A

Barbiturates

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60
Q

Can cause bradycardia and hypotension

A

Dexmedetomidine

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61
Q

What induction agent has most stable cardiovascular profile?

A

Etomidate

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62
Q

What induction agent increase BP, and cardiac output?

A

Ketamine

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63
Q

Explain the physiological response to the release of thromboxane and prostacyclin?

A

a. TXA2- platelet aggregation and vasoconstriction
b. Prostacyclin- inhibits platelet aggregation & vasodilates
c. these 2 work in a balance, if one is opposed, then the other can exert it’s intrinsic properties

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64
Q

What agent can be used to prevent ductus arteriosus closure (Keeps the PDA patent/open)?

A

a. Alprostadil (Prostin VR, Muse, PGE1)
b. Alprostadil can also give men boners (tx erectile dysfunction if the old lady isn’t doing it for us
anymore…)

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65
Q

Where can we see the use of Alprostadial?

A

a. Neonatal congenital heart defects
i. Cyanotic PPTT: Pulmonary atresia, pulmonary stenosis, tricuspid atresia, Tetralogy Of Fallot
ii. Acyanotic: Coarctation of aorta, hypoplastic LV (CH)

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66
Q

What agent can be used to close ductus arteriosis?

A

Indomethacin

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67
Q
  1. What effects will each prostaglandin have on SVR?

Prostacyclin (PGI2) Epoprostenal *Flolan – *

A

Decrease SVR, Increase PVR, Decrease Platelet

Aggregation

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68
Q

Epoprostenal *Flolan Treatment of

A

Primary Pulmonary HTN

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69
Q

What effects will each prostaglandin have on SVR? Alprostadil (PGE1)

A

Decrease SVR, Increases PVR, Decreases Platelet Aggregation, & Increase Uterine Tone *Keeps PFO open

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70
Q

What effects will each prostaglandin have on SVR? Iloporost (Nebulizer) –

A

Decrease SVR, Decrease PVR, Decrease Platelet Aggregation

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71
Q

Prostaglandins use as a nebulizer

A

Iloporost

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72
Q

What effects will each prostaglandin have on SVR? Thromboxane (TXA2)

A

Thromboxane (TXA2) – Increase SVR, Increases PVR, & Increases Platelet aggregation

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73
Q

What effects will each prostaglandin have on SVR? Dinoprost (PGF2)

A

Increase or Decrease SVR, Increase PVR, Increase Uterine Tone

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74
Q

Increases Uterine Tone ONLY

A

Dinoprostone (PGE2) –

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75
Q

3 agents used Increase uterine tone

A

Alprostadil
Dinoprost
Dinoprotone

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76
Q

What prostaglandin can be used to treat refractory post-partum bleeding? What is the dose?

A

Carboprost (Hemabate) a PGF-2α that produces uterine contractions? Dose = 250 mcg IM, repeat 1.5-3.5 min intervals

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77
Q

Carboprost Risks of this agent-

A

vomiting, diarrhea, hyperthermia

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78
Q

What are some characteristics of Prostaglandins?

A

a. Acidic lipids with great pharmacologic activities
b. Act as local hormones
c. Synthesized from arachidonic acid, dihydrolinoleic acid, & eicosapentaenoic acid

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79
Q

What causes the release of Arachidonic Acid?

A

Phospholipase C and A2

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80
Q

What drugs can we give to inhibit Phospholipase production inhibiting the Arachidonic acid pathway?

A

Corticosteroids

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81
Q

What is the half-time of Thromboxane A2?

A

30 seconds (shorter)

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82
Q

What is the half- time of Prostacyclin?

A

3 minutes (longer)

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83
Q

What component of prostaglandin synthesis has Several 1000x MORE POTENT bronchial smoothmuscle vasoconstriction than Histamine?

A

a. Leukotrienes *Therefore it is important to not give asthmatic patients high dose of aspirin or NSAIDs because you can push the phospholipase pathway down the lipoxygenase path producing more leukotrienes

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84
Q

All opioids antagonists

A

Narcan

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85
Q

What can NSAIDs do to the kidneys?

A

a. Inhibit cyclooxygenase, interfering with renal prostaglandins
b. Catecholamine induced renal vasoconstriction

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86
Q

What agents are used for cervical ripening prior to labor induction?

A

a. Dinoprostone; Cervidil, Prostin E2, Prepidil
b. Can be used during weeks 12-28 to evacuate the uterus after missed abortion or intrauterine fetal
death

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87
Q

What enzymes play a role in each step of prostaglandin synthesis?

A

a. Phospholipase A2 → Arachidonic Acid
i. Cyclooxygenase → Endoperoxides→
1. Thromboxane Synthetase→ Thromboxane (vasoconstriction & platelet agg.)
2. Prostacyclin Synthetase→ Prostacyclin (vasodilator & inhibits platelet agg.)
ii. Lipoxygenase → 5-hydroxyarachidonic acid→ Leukotrienes (1000x more potent
bronchoconstriction than Histamine)

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88
Q

4What is the mechanism of action of:Cromolyn:

A

Inhibits antigen-induced release of histamine and other autocoids (leukotrienes from
pulmonary mast cells, and other tissue mast cells). basophils.

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89
Q

Does Cromolyn prevent release of histamine form

A

NO

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90
Q

Does Cromolyn relax bronchial or vascular smooth muscle

A

No

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91
Q

What is the mechanism of action of antihistamines?

A

competitive antagonists- occupy receptors on effector cell membranes

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92
Q

Which H2 antagonist is associated with greatest risk of CYP-450 enzyme inhibition? What can it lead to ?

A

a. Cimetidine
b. Increases plasma concentration of Propranolol, Diazepam, & Lidocaine (all have hepatic extraction ratios & depend on microenzyme metabolism)

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93
Q

What are physiologic responses to histamine release?

H1 receptor physiologic response-

A

Smooth muscle contraction in GI and Pulmonary, induces NO release which stimulates guanylate cyclase to cause vasodilation, increase capillary permeability,
hypotension, tachycardia, flushing, headache, release of prostacyclin

94
Q

H2 receptor physiologic response

A

stimulation of gastric H+ secretion

95
Q

Increase myocardial contractility and HR

A

H2 receptor

96
Q

H3 receptor physiologic response-

A

inhibition of synthesis and release of histamine (Antagonism of H2 attenuates H3 function)

97
Q

Antagonism of H2

A

attenuates H3 function

98
Q

What is the result of blocking H2 receptor alone, followed by the administration of a histamine releasing drug?

A

An increase in release of histamine

99
Q

How do first generation antihistamines differ? What are examples of first and second generation antihistamines?

A

1st generation- more sedation, may also block muscarinic, serotonin, or alpha adrenergic (
diphenhydramine, promethazine

100
Q

What are examples of second generation antihistamines?

A

2nd generation- less sedation (fexofenadine, loratadine, cetirizine)

101
Q

Which generation antihistamine may also block muscarinic, serotonin, or alpha adrenergic?

A

1st

102
Q

Examples of first generation antihistamines are

A

Diphenhydramine

Promethazine

103
Q

Examples of 2nd generation antihistamines are

A

fexofenadine, loratadine, cetirizine)

104
Q
  1. Compare the potency of ketorolac to narcotics?
A

30 mg ketorolac IM = 10 mg morphine =100mg meperidine

105
Q

What dose of aspirin is required to inhibit the cox-1 enzyme?

A

75-325mg

106
Q

What is the recommended dose of ketorolac?

A

30 mg

107
Q

What is the recommended dose of ketorolac in a 65 y.o patient?

A

Do not exceed 30 mg in elderly for loading dose and don’t exceed 15 mg for maintenance

108
Q

What is the recommended dose of IV acetaminophen?

A

a. <50kg: 12.5mg/kg q 4 hours OR 15 mg/kg q 6h Pediatrics

b. >50kg: 650 mg q 4 hours OR 1 gram q6h

109
Q

Infusion time for IV acetaminophen (Ofirmev)?

A

Over 15 minutes

110
Q

What coagulation test can be used to monitor aspirin?

A

a. Bleeding time? prothrombin time? Platelet function?

111
Q

What is the mechanism of action of corticosteroids?

A

Block phospholipase A2 from producing arachidonic acid

112
Q

What are adverse reactions from NSAIDs?

A

a. Most common: Dyspepsia, Renal adverse effects, Peptic ulcer less common
b. Other: skin rxn, CNS effects, postop bleeding
c. Rare: blood dyscrasias, uticaria, erythema multiform, pneumonitis, aseptic meningitis

113
Q

PUD may be a side effect of ______And it is ____common

A

NSAIDS, less

114
Q

Most common side effect of NSAIDS

A

Dyspepsia

115
Q

What are the clinical properties of acetaminophen?

A

a. Mild/moderate analgesic, antipyretic, low gastric irritation & platelet aggregation
b. NO ANTI-INFLAMMATORY PROPERTIES!!!!

116
Q

What are clinical effects of aspirin?

A

Analgesic, antipyretic, platelet inhibition (for the life of the platelet ~ 7 days)

117
Q

How long should aspirin be held prior to elective surgery?

A

7-10 days

118
Q

What agents can be used to treat an acute gout attack?

A

Colchicine

119
Q

Does Tylenol have anti-inflammatory effects?

A

NO

120
Q

What are physiological effects of high and low dose aspirin?

A

a. High dose: anti-inflammatory dose 2.5-5.4 g/day

b. Low dose: MI prophylaxis 75-325 mg/day, analgesic/antipyretic 325-650 mg q 4-6 hours

121
Q

What patients are at highest risk from aspirin associated bronchospasms? What is the cause of this reaction?

A

a. Asthma pts- increases availability of arachidonic acid for production of leukotrienes

122
Q

Define the role of NSAIDs for the treatment of post-operative pain.

A

Decreases postop pain,and requirements (20-50%), not used as sole treatment,
should be combined with short-acting opioids or LA, less N/V than with opioids alone

123
Q

What are the maximum recommended doses With Epi and Without for:

A

Etidocaine- 400 mg, 300mg (Not used for spinals)

124
Q

What are the maximum recommended doses With Epi and Without for:. Bupivacaine-

A

225 mg, 175 mg

125
Q

For Bupivacaine, Intervals must be

A

> 3 hours & Max dose in 24 hrs = 400 mg

126
Q

For Bupivacine, OB continuous epidurals:

A

if 0.5% solution plain (no epi) limit dose to 320 mg

127
Q

What are the maximum recommended doses With Epi and Without for:

A

Lidocaine- 7 mg/kg (500mg total), 4.5 mg/kg (300mg total)

128
Q

What are the maximum recommended doses With Epi and Without for

A

Chloroprocaine – 14 mg/kg (1000 mg total), 11 mg/kg (800 mg total)

129
Q

What are the maximum recommended doses With Epi and Without for: Procaine

A

Procaine (Novocaine) – Max 1000 mg

130
Q

What is the maximum recommended dose of prilocaine (EMLA)?

A

a. Max 600 mg

b. O-toludine = Methemoglobin

131
Q

Which local anesthetic best demonstrates a differential block?

A

bupivacaine

132
Q

What will result when bicarbonate is added to a local anesthetic solution?

A

a. Speeds onset

b. Can form a precipitate, so need to use right away

133
Q

What effect will adding bicarbonate to LA have this have on onset of action?

A

LA will become mostly non-ionized with higher pH of surrounding solution

134
Q

What concentration of bupivacaine is not recommended by the FDA in OB?

A

0.75% = known to have CV toxicity and arrest

135
Q

Which local anesthetic has greatest cardiac toxicity?

A

Bupivicaine

136
Q

This LA is not used for spinal

A

Etidocaine

137
Q

What are signs/symptoms of CNS toxicity?

A

Circumoral numbness, lightheadedness, tinnitus, visual disturbances, slurring of speech, muscle twitching, unconsciousness, grand mal seizures, coma, apnea

138
Q
  1. What is the order of nerve blockade by local anesthetics? What are the clinical signs of the order of
    nerve blockade by local anesthetics?
    a. 1st:

c. 3
d. 4th: A-beta (sensory/proprioception, touch, pressure)
e. 5th: A-alpha (motor, skeletal muscle, proprioception)

A 
B fibers, C fibers and 
A delta fibers
A gamma
A beta
A alpha
139
Q

B fibers

A

preganglionic autonomic

140
Q

A-delta

A

fast pain & temp

141
Q

C fibers

A

slow pain, temp, touch and

142
Q

Slow pain, temp, touch which fiber

A

C fibers

143
Q

Postganglionic autonomics, which fiber

A

C fibers

144
Q

A-gamma action

A

muscle tone, motor, reflexes

145
Q

A-beta

A

sensory/proprioception, touch, pressure

146
Q

A-alpha

A

motor, skeletal muscle, proprioception

147
Q

First fibers blocked

A

B fibers

148
Q

What was the first Local anesthetics

A

Cocaine

149
Q

What is a metabolite of ester local anesthetics?

A

a. Paraaminobenzoic acid (PABA)

150
Q

What is the primary determinant of the potency,of local anesthetics?

A

lipid solubility

151
Q

What is the primary determinant of onset of LA?

A

IONIZATION

152
Q

What is the primary determinant of duration of action of LA ?

A

Protein binding

153
Q

What should be done at the first sign of suspected CNS local anesthetic toxicity?

A

a. Restlessness, vertigo, tinnitus, & difficulty focusing occur initially

154
Q

Primary concern with CNS toxicity with LA

A

seizures- maintain airway and oxygenate patient

155
Q

Non-CNS LA toxicity- can have patient

A

hyperventilate

156
Q

Which local anesthetic is recommended for an emergency C-section?

A

Chloroprocaine (ester LA, least toxicity known to man, good for epidural, but NOT for spinal d/t NO plasma esterases in CSF to metabolize so it depends highly on redistribution for metabolism)

157
Q

What is the mechanism of action of local anesthetics?

A

Block fast Na channels (greater affinity for open or inactive

158
Q

2 states of Na channel LA work on

A

Open or Inactive

159
Q

What local anesthetic can cause methemoglobinemia?

A

Prilocaine, Benzocaine, Cetacaine, Lidocaine

160
Q

What are causes of increase in the minimal blocking concentration for local anesthetics?



A

Increase nerve fiber diameter, increase myelination, greater distance b/w nodes of Ranvier

161
Q

What is the diameter of each nerve fiber A-alpha:

A

15-20 microns (largest)

162
Q

What is the diameter of each nerve fiber. A-beta:

A

5-12 microns

163
Q

What is the diameter of each nerve fiber. A-gamma:

A

3-6

164
Q

What is the diameter of each nerve fiber A-delta:

A

1-4 (pain)

165
Q

What is the diameter of each nerve B fibers:

A

<3

166
Q

What is the diameter of each nerve fiber C fibers

A

0.3-1.3 (smallest) (pain)

167
Q

How many nodes of Ranvier must be blocked to inhibit nerve conduction?

A

2-3

168
Q

How are local anesthetics metabolized?Amides

A

Liver

169
Q

How are local anesthetics metabolized?Esters

A

Plasma cholinesterases

170
Q

What local anesthetics are classified as amides?

A

they all contain 2 “i” Prilocaine>etidocaine>lidocaine>mepivicaine>bupivacaine

171
Q

What local anesthetics are classified as esters?

A

They all contain 1 “i”

Chloroprocaine>procaine>tetracaine>Cocaine

172
Q

How does cocaine differ from other ester local anesthetics?

A

Vasoconstrictor, metabolized by liver & plasma esterases.

173
Q

Only ester metabolized by the liver is

A

Cocaine

174
Q

Cocaine and neurotransmitter

A

Also is a sympathomimetic increasing post-synaptic NE and; Dopamine

175
Q

Which local anesthetic can be used to treat recalcitrant (resistant) seizure activity?

A

Lidocaine

176
Q

What is recommended treatment for local anesthetic cardiac toxicity?

A

Intralipid therapy 20%

177
Q

Which local anesthetic will NOT cause vasodilatation?

A

Cocaine & Mepivacaine

178
Q

Why is epinephrine added to local anesthetic solutions? What are PROS of epinephrine use?

A

Decreases absorption of LA & prolongs the effects, decreases systemic toxicity, permits higher doses of LA

179
Q

Cons of EPI use with LA

A

Tachycardia, do not use with patient who are tachycardic?

180
Q

Know potencies of the local anesthetics.O:Water P/C

A

The higher the oil:water p.c., the more potent

181
Q

Potency of LA

A

Bupivacaine=tetracaine>ropivacaine>etidocaine>lidocaine=mepivacaine>chloroprocaine (B=
TREL=MC)

182
Q

Onset of absorption, for most to least (ITIC PEBSS)

A

IV>tracheal>intercostal>caudal>paracervical (pudendal block)>epidural>Brachial Plexus>SubArachnoid/Sciatic/Femoral>SQ (ITIC PEBSS)

183
Q

What is the selectivity in cardiac toxicity of LA?

A

a. Bupivacaine > Etidocaine > Lidocaine

184
Q

FIRST SIGN of LA toxicity

A

Circumoral numbness (mouth, lip, tongue)

185
Q

What are the 3 characteristics segments of Local anesthetics?

A 
Aromatic ring (lipophillic)
Intermediate Carbon group (ester or amide) 
Tertiary amine (hydrophillic)
186
Q

What clotting factor is deficient in patients with: Hemophilia A-

A

Factor VIII deficiency

187
Q

What clotting factor is deficient in patients with:

A

Hemophilia B- Factor IX deficiency (Christmas factor)

188
Q
  1. What laboratory test are abnormal in a patient with:

a. Hemophilia A-

A

normal PT, abnormal aPTT, the specific factor assay for factor VIII will reveal
the appropriate defect. Should undergo test for vWB

189
Q

What laboratory test are abnormal in a patient with Hemophilia B-

A

normal PT, abnormal aPTT, specific assay for factor IX

190
Q

What laboratory test are abnormal in a patient with Hemophilia Bm-

A

both PT & aPTT prolonged

191
Q

How should a patient with inhibitors for factor VIII or factor IX be managed prior to elective surgery?

A

Reduce inhibitor levels with immunosuppressant therapy (cyclophosphamide), gamma-globulin, plasmapheresis, or by tolerance with high dose or frequent administration of factors

192
Q

What products are recommended for the prevention of bleeding in a patient with Von Willibrand’s
disease?

A

Cryoprecipitate, Humate-P, Koate-HS and Koate HP have been reported to achieve clinical
hemostasis prior to surgery and can be used in place of cryoprecipitate

193
Q

Goals of therapy for VWD are to

A

improve factor VIII levels, and improve bleeding time

194
Q

What is the recommended treatment for mild bleeding associated with VWB disease?

A

Desmopressin 0.3-0.4 mcg/kg, infuse over 15 minutes may be given to treat mild bleeding episodes

195
Q

What are most common adverse effects associated with desmopressin?

A

Facial flushing (most common)

196
Q

DDAVP can cause

A

platelet aggregation and severe thrombocytopenia

197
Q

DDAVP Used in type

A

IIb vWB

198
Q

Less Frequent SE of DDAVP:

A

Mild H/A, increase HR, decrease BP (you wouldn’t think), water retention which may lead to severe hyponatremia, increase plasminogen activator

199
Q

What agent can be given to inhibit the potential fibrinolysis from DDAVP?

A

Aminocarproic acid

200
Q

What is goal concentration of factor VIIIX prior to surgery?

A

Desired factor VIII levels 1 hour prior to surgery 100%, then 50% until wound healing begins, then 30% until complete would healing

201
Q

What is goal concentration of factor IX prior to surgery?

A

Half-life of factor IX is 24 hours, with normal hemostasis occurring when plasma levels area about 10-25%

202
Q

What are signs/ symptoms of Class I hemorrhage?

Class I

A

loss of up to 15% of total blood volume. Causes vasoconstriction and mild tachycardia.

203
Q

What are signs/ symptoms of Class II hemorrhage?

Class II

A

loss of 15-30% of blood volume, produces tachycardia, decreased pulse pressure,anxiety, restlessness

204
Q

Class I and II hemorrhages, How should these patients be managed?

A

IV crystalloid therapy

205
Q

What are the signs/symptoms of Class III hemorrhage?

Class III-

A

loss of 30-40%. Produces hypovolemia, marked tachycardia, systolic hypotension, AMS.

206
Q

What are the signs/symptoms of Class IV hemorrhage?Class IV

A

more than 40% of total blood volume is life threatening and accompanied by marked tachycardia and very narrow pulse pressure, and low urine output. Mental status markedly depressed.

207
Q

Class III and IV hemorrhages, How should these patients be managed?

A

In young, healthy patient, up to 30-40% of blood volume usually can be treated adequately with
crystalloid therapy

208
Q

What are the indications for the administration of platelets?
d. Determination of whether pts with intermediate (50,000-100,000) require therapy should be
based on risk of bleeding

A

Transfusion of one platelet concentrate will increase the platelet count by approximately 5,000- 10,000 in an average adult.

209
Q

Usual therapeutic dose is (for platelet)

A

1 platelet concentrate per 10kg body weight

210
Q

Prophylactic platelet transfusion

A

is rarely indicated in surgical platelet with thrombocytopenia d/t decreased platelet production when platelet count is >100,000 and is usually indicated when <50,000.

211
Q

What are the indications for administration of packed RBCs?Transfusion is rarely indicated when

A

Hgb concentration is >10g/dL

212
Q

Transfusion is Almost always indicated when it

A

is less than 6g/dL, especially when anemia is acute

213
Q

Transfusion 1 unit whole PRBCs increases

A

Hct 3% or Hgb 1g/dL, in a 70 kg non-bleeding adult

214
Q

What are the indications for the administration of FFP?

A

a. Urgent reversal of warfarin therapy

b. Microvascular bleeding with elevated PT or PTT (>1.5 times normal)

215
Q

What is the most common inheritable coagulopathy?

A

Von Willebrand Disease

216
Q

VWD Results in

A

abnormal platelet function & defective for plasma clotting

217
Q

What is VWD, needed for

A

factor VIII complex, stimulates VIII production

218
Q
  1. When should we not use DDAVP, in what type of Von Willebrand Disease?
A

Type 2B

219
Q

Can ause platelet aggregation & severe thrombocytopenia

A

DDAVAP

220
Q

Never use DDAVP in the beginning of presumed Von Willebrand Disease for this reason why?

A

because different sub-types exist and require different treatment modalities

221
Q

Relative clinical potency and BUPIVACAINE Oil/ water partition

A

8;30

222
Q

Relative clinical potency and Tetracaine Oil/ water

A

8; 80

223
Q

Relative clinical potency and Lidocaine Oil/ water partition

A

2;4

224
Q

Relative clinical potency and Mepivacaine; Oil/ water partition

A

2; 1

225
Q

Relative clinical potency and chloroprocaine; Oil/ water partition

A

1;1

226
Q

Lidocaine primary metabolite is

A

Monoethylglyceinexylidide (use to assess hepatic functions to predict morbidity and mortality)

227
Q

Prilocaine hepatic derived metabolite

A

O-Toluidine

228
Q

Define minimum blocking concentration (Cm)

A

The lowest concentration of drugs needed for blocking impulse propagation. think of it like MAC for local anesthetics

229
Q

A patient is known to be allergic to penicillin.This patient may be allergic to what other an,bio,cs?

A

Cephalosporins (Cross-reac,vity 5%) among beta-lactams

230
Q

Is there cross-sensitivity among ester local anesthetics? •

A

There is cross reactivity among ester LA. Due to common metabolite para-aminobenzoic
acid.

231
Q

Between ester and amide anesthetics?

A

No

SRNAPharmacology II (32 decks)

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